neuro Flashcards
(93 cards)
GBS: define and aetiology
an acute (quick onset) paralytic polyneuropathy → affects PNS
An acute inflammatory demyelinating ascending polyneuropathy affecting the PERIPHERAL NERVOUS SYSTEM (SCHWANN CELLS TARGETED) following an upper respiratory tract infection of GI infection
triggered by infection
- Campylobacter jejuni
- Cytomegalovirus (CMV)
- Epstein-Barr virus (EBV)
GBS: pp?
- GBS is usually triggered by infection e.g. Campylobacter jejuni, EBV or cytomegalovirus (CMV)
- infectious organisms share the same antigens as those on the Schwann cells (PNS) so the antibodies made (by B cells) against the infectious organisms will also WORK AGAINST the schwann cells or against axon itself - MOLECULAR MIMICRY→ leading to autoantibody mediated nerve cell damage formation via molecular mimicry
- Nerve cell damage consists of damage to the SCHWANN CELLS and thus demyelination resulting in the reduction in peripheral nerve conduction resulting in an acute polyneuropathy
GBS: symptoms?
-
1-3 weeks post infection
- symptoms peak within 2-4wks
- slow recovery per
- iod lasting months-yrs
- a SYMMETRICAL ASCENDING MUSCLE WEAKNESS starts - this may advance quickly, affecting all limbs at once and
can lead to paralysis - can also affect sensory nerves = → sensory neuropathy - can be peripheral loss of sensation or neuropathic pain
- Reduced reflexes bc its a peripheral neuropathy- Reflexes are lost early in the illness
GBS: investigations?
made clinically - no specific test
- brighton criteria
supported by:
-
Nerve conduction studies (NCS):
• DIAGNOSTIC if matches with clinical examination
• Show slowing of conduction, prolonged distal motor latency +/- conduction block - baso shows reduced signal throughout the nerve -
Lumbar puncture - done at L4:
• CSF has raised protein but normal white cell count
GBS: management?
-
IV IMMUNOGLOBULIN for 5 days:
• Decreases the duration and severity of paralysis
• Contraindicated in patients with IgA deficiency!! - in whom it can cause a severe allergic reaction - screen for deficiency BEFORE treatment - Plasma exchange
- Supportive care
- venous thromboemblism prophylaxis ie Low-molecular weight heparin e.g. SC ENOXAPARIN and compression stockings to reduce risk of venous thrombosis - to prevent them from getting blood clots bc PE is major causse of death in GBS
If FVC < 1.5L/80% / if there is respiratory failure then ventilate and admit to ICU- MONITOR FVC 4 HOURLY!
ACA stroke: symptoms?
- Lower limb weakness and loss of sensation to the lower limb.
- Gait apraxia (unable to initiate walking).
- Incontinence.
- Drowsiness.
- Difficulty initiating speech
PCA stroke: symptoms?
- Visual field defects.
- Cortical blindness.
- Visual agnosia.
- Prosopagnosia.
- Dyslexia.
- Unilateral headache.
MCA stroke: symptoms?
CONTRALATERAL ARM & LEG WEAKNESS
• CONTRALATERAL sensory loss
• Hemianopia
• Aphasia (inability to understand or produce speech)
• Dysphasia (deficiency in speech generation)
• Facial droop
Meningitis: management?
-
children seen in community/primary care w suspected meningitis AND non-blanching rash
- URGENT STAT INJECTION (IM or IV) of benzylpenicillin
- IF YOU SUSPECT BACTERIAL MENINGITIS - START ANTIBIOTICS BEFORE TESTS COME BACK!!(steroids then ab?)
- < 3 months–IV cefotaximeplusamoxicillin(the amoxicillin is if its listeria monocytogenes - to cover listeria contracted during pregnancy from the mother)
- > 3 months–IV ceftriaxone
Vancomycin- for return travellers
ORAL Dexamethasone— Steroidsare also used in bacterial meningitis to reduce the frequency and severity ofhearing lossandneurological damage/cerebral oedema.
Meningitis: prevention?
Post exposure prophylaxis is guided bypublic health. The usual antibiotic choice for this is asingle doseofciprofloxacin!!!
prophylaxis is only EFFECTIVE AGAINST N.meningitidis.
This risk of highest for people that have had close prolonged contact within the7 daysprior to the onset of the illness. T
Meningitis: investigations
- Physical exam
- Blood cultures BEFORE LUMBAR PUNCTURE
- Blood tests; FBC, U&E, CRP, serum glucose, FOR SEROLOGY + PCR
- Throat swabs (bacterial + viral)
-
Lumbar puncture at L4 - measure pa and analyse WBC, protein and glucose - if unable to perform within 30 mins give empirical antibiotics!:
. It makes sense that bacteria swimming in the CSF will release proteins and use up the glucose. Viruses don’t use glucose but may release a small amount of protein. The immune system releases neutrophils in response to bacteria and lymphocytes in response to viruses.
CT head:
• To exclude lesions e.g. tumour
Meningitis: symptoms? triad?
Headache + neck stiffness + fever
in acute bacterial infection:
Onset is typically sudden
- Papilloedema:
- fever (pyrexia) rigors, severe headache, photophobia and vomiting - within hours
or minutes
- Neck stiffness, positive Kernig’s & Brudzinski’s
sign can appear within hour
- Meningococcal septicaemia is associated with a
NON-BLANCHING PETECHIAL (test using glass
test) + PURPURIC SKIN RASH
Meningitis: aetiology
most common cause of viral meningitis = Enterovirus.
bacteria and viruses → = ACUTE meningitis
fungi = CHRONIC MENINGITIS
Adults and children:
• Neisseria meningitides - gram-NEGATIVE DIPLOCOCCI - transmitted by droplet spread
• Streptococcus Pneumoniae/Pneumococcus
- Pregnancy women/older adults:
• Listeria monocytogenes - found in cheese, why pregnant women told to AVOID- also strep menominiae
Neonates:
• Escheria coli
• Group B Haemolytic streptococcus
Encephalitis: management?
If viral e.g. herpes simplex or varicella zoster then IMMEDIATE TREATMENT with anti-viral e.g. IV ACICLOVIR - even BEFORE the investigation results are available
- Anti-seizure medication e.g. PRIMIDONE
- If meningitis is suspected then EMERGENCY IM BENZYLPENICILLIN
Encephalitis: investigations?
-
Lumbar puncture:
- Lymphocytosis (raised lymphocytes).
- Raised protein.
- Normal glucose.
MRI:
• Shows areas of inflammation and swelling, generally in the temporal
lobes in HSV encephalitis
Encephalitis: symptoms? triad?
triad: Fever + Headache + Altered mental status/Behavioural Change +/- lethargy
-
Begins with features of viral infection:
- Fever, headaches, myalgia, fatigue and nausea
-
Progresses to:
- Personality and behavioural changes - common early manifestation
- Decreased consciousness, confusion, drowsiness
Seizures#
- Focal neurological deficit:
- Hemiparesis and dysphasia
WHOLE BRAIN AFFECTED - THUS problems with consciousness (global defect in higher functioning as well as drowsiness etc.) compared to meningitis
Encephalitis: define and aetiology? and epidemiolgy?
- Infection and inflammation of the brain parenchyma
- Usually viral
epidemiology =
- Infections are most frequent in children and elderly - mainly viral cause
- More common in immunocompromised
-
Mainly viral:
• Herpes simplex virus 1 & 2
• Varicella zoster, Epstein Barr, Cytomegalovirus, HIV, mumps, measles - Non-viral:
• Bacterial meningitis
• TB
• Malaria
Huntington’s: typical age and pp?
Patients are usually asymptomatic until symptoms begin around aged 30 to 50.
Huntington’s is a cause of chorea and is a neurodegenerative disorder
characterised by the LACK of the inhibitory neurotransmitter GABA
Huntington’s chorea is anautosomal dominantgenetic condition that causes a progressive deterioration in the nervous system.
Huntington’s: symptoms?
define chorea
A continuous flow of jerky, semi-purposeful movements, flitting from one
part of the body to another
• They may interfere with voluntary movements but cease during sleep
BEGINS:
- cognitive,psychiatric ormood, or behavioural problems
- Irritability.
- Depression.
- Personality change.
FOLLOWED BY:
-
Chorea(involuntary, abnormal movements)
- Relentlessly progressive, jerky, explosive, rigidity INVOLUNTARY
movements - CEASES when sleeping - Can’t sit still
- May begin as general restlessness, unintentionally initiated
movements and lack of coordination
- Relentlessly progressive, jerky, explosive, rigidity INVOLUNTARY
- Eye movement disorders
- Speech difficulties (dysarthria)
- Swallowing difficulties (dysphagia)
- Dementia: Impaired cognitive abilities and memory
Huntington’s: management?
SUPPORTING PERSON AND FAMILY:
There is no treatment to prevent progression
MEDS - for SYMPTOMATIC RELIEF:
- Symptomatic management of chorea:
• BENZODIAZEPINES EG diazepam
• Antipsychotics (e.g. olanzapine) • SULPIRIDE - neuroleptic - depresses nerve function
• TETRABENAZINE - dopamine depleting agent -
Antidepressants such as selective serotonin reuptake inhibitors (SSRI’s)
e.g. SEROXATE -
Counselling to patient and family, genetic counselling to any children of
patients - Speech and language therapywhere there are speech and swallowing difficulties
- Advanced directivesto document the patients wishes as the disease progresses
- End of lifecare planning
Parkinson’s: define and triad of symptoms?
Degenerative movement disorder caused by a REDUCTION IN DOPAMINE IN THE SUBSTANTIA NIGRA (in the basal ganglia of the brain)
Characterised by the triad of:
- Rigidity
- Bradykinesia (slow to execute movement)
- Resting tremor
Parkinson’s: 2 histopathological signs of Parkinson’s disease.
also pp?
- Lewy bodies.
-
Loss of dopaminergic neurones in the substantia nigra.
- The substantia nigra produces DOPAMINE→ In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine.There is a loss of dopamine producing neurones in the substantia nigra.
Parkinson’s: symptoms?
Onset is ASYMMETRICAL - ONE SIDE ALWAYS WORSE THAN THE OTHER
Characterised by the triad of:
- Rigidity
pain, problems turning in bed
is a resistance to passive movement of a joint.
Bradykinesia (slow to execute movement)can only take small steps when walking (“shuffling gait”)
reduced facial movements and expressions - expressionless face (hypomimesis)
-
Resting tremor
-
Improved by voluntary movements and made worse by anxiety/if pt is distracted
requency of 4-6 Hz, meaning it occurs 4-6 times a second - pill rolling tremor”
-
Improved by voluntary movements and made worse by anxiety/if pt is distracted
REM sleep disorders
Depression is common, psychiatric problems, dementia
Stooped posture,
loss of sense of smell
Parkinson’s: management?
Main treatment aim is to compensate for the loss of dopamine - ie to increase dopamine levels
Due to all the above complications, L-Dopa should only be started until
ABSOLUTELY NECESSARY - when other treatments are ineffective
—— BUT dopamine can’t cross BBB so given PO L-DOPA or LEVODOPA which is a synthetic dopamine that can cross BBB but does have s/e
- —- usually combined with peripheral decarboxylase inhibitors - Examples arecarbidopa andbenserazide
- Co-benyldopa (levodopaand***benserazide
- Co-careldopa (levodopaand***carbidopa
ENTACAPONE - COMT Inhibitors!!! These are inhibitors ofcatechol-o-methyltransferase(COMT) - These inhibit COMT which breaks down dopamine
Dopamine Agonist - eg Bromocryptine, Pergolide, Carbergoline
usually used to delay the use of levodopa and are then used in combination with levodopa
Monoamine Oxidase-B Inhibitors - eg selegiline, rasagiline
physiotherapy
Physical activity